Fluoxetine protects against inflammation and promotes autophagy in mice model of post-traumatic stress disorder

Lou, Chengjian; Fang, Marong; Ye, Shan; Fang, Zhanglu; Amin, Nashwa; Chen, Yili

doi:10.1016/j.bbr.2022.114004

Cited by 7 publications

(2 citation statements)

References 31 publications

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“…IL-1β and other cytokines, such as IL-6, are increased in the brain in animal models of PTSD [ 173 , 174 , 175 ]. Moreover, IL-1β activates p38 MAPK in astrocytes and hippocampal neurons [ 176 ], a pathway linked to synaptic plasticity that contributes to hippocampal NMDAR-dependent long-term depression (LTD), thereby influencing long-term memory in vivo [ 177 ].…”

Section: Nnos No-related Mechanisms and Stress Responsementioning

confidence: 99%

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

Fronza,

Ferreira,

Pavan-Silva

et al. 2023

Molecules

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Post-traumatic stress disorder (PTSD) is a psychiatric condition characterized by persistent fear responses and altered neurotransmitter functioning due to traumatic experiences. Stress predominantly affects glutamate, a neurotransmitter crucial for synaptic plasticity and memory formation. Activation of the N-Methyl-D-Aspartate glutamate receptors (NMDAR) can trigger the formation of a complex comprising postsynaptic density protein-95 (PSD95), the neuronal nitric oxide synthase (nNOS), and its adaptor protein (NOS1AP). This complex is pivotal in activating nNOS and nitric oxide (NO) production, which, in turn, activates downstream pathways that modulate neuronal signaling, including synaptic plasticity/transmission, inflammation, and cell death. The involvement of nNOS and NOS1AP in the susceptibility of PTSD and its comorbidities has been widely shown. Therefore, understanding the interplay between stress, fear, and NO is essential for comprehending the maintenance and progression of PTSD, since NO is involved in fear acquisition and extinction processes. Moreover, NO induces post-translational modifications (PTMs), including S-nitrosylation and nitration, which alter protein function and structure for intracellular signaling. Although evidence suggests that NO influences synaptic plasticity and memory processing, the specific role of PTMs in the pathophysiology of PTSD remains unclear. This review highlights pathways modulated by NO that could be relevant to stress and PTSD.

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Section: Nnos No-related Mechanisms and Stress Responsementioning

confidence: 99%

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

Fronza,

Ferreira,

Pavan-Silva

et al. 2023

Molecules

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“…A single prolonged stress (SPS) protocol, besides modeling a post-traumatic stress disorder, causes neuroinflammation in male mice [ 16 ]; therefore, the rationale to choose resistance exercise over other modalities of aerobic exercise is that aerobic exercise has been reported as potentially inflammatory, whereas, resistance exercise has been related to an anti-inflammatory pattern [ 17 ]. Acknowledging the potential benefits of exercise, this study evaluated if resistance exercise protects against anxiety-depression-like dyad in mice subjected to an emotional single prolonged stress ( Esps ) protocol.…”

Section: Introductionmentioning

confidence: 99%

Resistance Training Modulates Hippocampal Neuroinflammation and Protects Anxiety-Depression-like Dyad Induced by an Emotional Single Prolonged Stress Model

et al. 2022

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Stress is a triggering factor for anxious and depressive phenotypes. Exercise is known for its action on the central nervous system. This study aimed to evaluate the role of resistance exercise in an anxiety-depression-like dyad in a model of stress. Male Swiss mice (35-day-old) were exercised, three times a week for 4 weeks on nonconsecutive days. The resistance exercise consisted of climbing a 1-m-high ladder 15 times. After mice were subjected to an emotional single prolonged stress (E sps ) protocol. Seven days later, they were subjected to anxiety and depression predictive behavioral tests. The results showed that exercised mice gain less weight than sedentary from weeks 3 to 5. Resistance exercise was effective against an increase in immobility time in the forced swim test and tail suspension test and a decrease in grooming time of mice subjected to E sps. Resistance exercise protected against the decrease in the percentage of open arms time and open arm entries, and the increase in the anxiety index in E sps mice. Four-week resistance exercise did not elicit an antidepressant/anxiolytic phenotype in non-stressed mice. E sps did not alter plasma corticosterone levels but increased the hippocampal glucocorticoid receptor content in mice. Resistance exercise protected against the decrease in hippocampal levels of tropomyosin kinase B (TRκB), the p-Akt/Akt, and the p-mTOR/mTOR ratios of E sps mice. Resistance exercise proved to be effective in decreasing hippocampal neuroinflammation in E sps mice. Resistance exercise protected against the increase in the hippocampal Akt/mTOR pathway and neuroinflammation, and anxiety/depression-like dyad in E sps exposed mice. Supplementary Information The online version contains supplementary material available at 10.1007/s12035-022-03069-x.

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Post-traumatic Stress Disorder: Focus on Neuroinflammation

Tong

Schock

et al. 2023

Mol Neurobiol

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Fluoxetine protects against inflammation and promotes autophagy in mice model of post-traumatic stress disorder

Cited by 7 publications

References 31 publications

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

“NO” Time in Fear Response: Possible Implication of Nitric-Oxide-Related Mechanisms in PTSD

Resistance Training Modulates Hippocampal Neuroinflammation and Protects Anxiety-Depression-like Dyad Induced by an Emotional Single Prolonged Stress Model

Post-traumatic Stress Disorder: Focus on Neuroinflammation

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